During ischemia, the administration of excess homocysteine causes the formation of s-adenosylhomocysteine (SAH) from adenosine, via the enzyme SAH hydrolase, at a rate that reflects the intracellular adenosine concentration. Since homocysteine can be labeled with the positron emitter 11C, the detection of 11C-SAH by positron emission tomography (PET) shows promise as a clinical tool for identifying impaired myocardial energy balance noninvasively. The general hypothesis of this proposal is that quantitative PET imaging using 11C-HCTL can be used to identify regional myocardial energy imbalance during ischemia.